PS120 Psychopathology Term 2 Part 2 Flashcards

1
Q

Paradigm

A
  • A conceptual framework or approach within which a scientist works
  • Paradigms often involve a concept or view of human nature
  • A paradigm has profound implications for which questions scientists ask and
    which answers they give
  • Proposed treatment procedures differ according to the paradigms within which
    they are set up
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2
Q

Defining Mental Disorder

A

Personal distress
Violation of Social Norms
Disability and dysfunction

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3
Q

Personal distress

A
  • Personal distress
  • Personal distress can be part of the definition of mental disorder
  • For instance: Anxiety and Depression
    → Not all disorders involve distress
  • e.g., antisocial type of personality
    → Not all psychological distress is related to a mental disorder
  • e.g., grief after death of a loved one
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4
Q

Violation of social norms

A
  • Violation of social norms
  • Social norms: Widely held standards defining what is considered to be normal
    behaviour in a particular situation
  • Behaviour that violates social norms might be classified as disordered
  • e.g., the conversation with imaginary voices that some people with schizophrenia engage in
    → Not all disorders involve violation of social norms
  • (e.g., individuals with some anxiety disorders rather rarely
    violate social norms)
    → Not all violations of social norms are related to mental
    disorder
    → Consider: Social norms vary a great deal across cultures and ethnicities
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5
Q

Disability and dysfunction

A
  • Disability
  • Impairment in some important area of life: social or occupational disability
  • e.g., substance use disorders are defined in part by the social or occupational disability
    → Not all disorders involve disability
  • e.g., many people with bulimia lead lives without impairment, while binging and purging in
    private
  • Dysfunction
  • Psychological processes not functioning in normal way
    (e.g., someone hears voices when objectively there are none)
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6
Q

What is psychological disorder?

A
  • The disorder occurs within the individual
  • It involves clinically significant difficulties in thinking, feeling, or behaving
  • It usually involves personal distress of some sort, such as in social relationships or
    occupational functioning
  • It is not a culturally specific reaction to an event (e.g., death of a loved one)
  • It is not primarily a result of social deviance or conflict with society
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7
Q

Stigma

A

A label is applied to a group of people that distinguishes individuals with a mental illness from
others (e.g., “crazy”).
* The label is linked to deviant or undesirable attributes by society (e.g., crazy → dangerous).
* People with the label are seen essentially different from those without.
* People with the label are discriminated against unfairly (e.g., “a clinic for crazy people should
not be built in our neighbourhood”).

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8
Q

Ancient Times - psychology

A

Early demonology: Ancient times
* Before the age of scientific inquiry all good and bad manifestations of power
beyond human control were regarded as supernatural
* Behaviour seemingly outside of individual control was also ascribed to
supernatural causes
* The doctrine that an evil being or spirit can
dwell within a person and control his/her mind
→ Demonology
Early treatments involved exorcisms and trephination.

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9
Q

Hippocrates - Early biological explanations

A
  • Hippocrates separated medicine from religion, magic, and superstition
  • E.g., seizures are not sacred
  • The brain as the organ of consciousness, intellectual life, emotions
  • Content of dreams may be symbolic
  • Three categories of mental illness:
  • Mania, melancholia and phrenitis
  • depended on a delicate balance of four humors/fluids
  • an imbalance of these humors produce mental illness
  • blood, black bile, yellow bile and phlegm
  • The treatments were quite different from exorcism
  • E.g., melancholia: prescribing tranquility, sobriety, care in choosing food and drink, and
    abstinence from sexual activity
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10
Q

Plato - Soul and mental illness

A
  • Plato (427 – 347 BC) soul as two-horse chariot
  • Reason is the driver
  • The two horses are:
  • Spirit (noble emotions)
  • Appetite (base drive)
    → Imbalance leads to mental illness
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11
Q

The Dark Ages and Demonology

A

The Dark Ages and Demonology (2nd – 17th century)
* Dark ages in Western European medicine and
treatment/investigation of mental disorder
* Christian monasteries replaced physicians as
healers/authorities on mental disorder
* The church gained influence
* Return to a belief in supernatural causes of
mental disorders
* The persecution of certain groups (non-Christians,
devil worshippers, witches)

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12
Q

Robert Burton (1577-1640)

A
  • “Anatomy of melancholy” (1621)
  • Comprehensive treatise containing personal disclosure
  • Causes and symptoms of melancholy
  • Good food, exercise
  • Laughter, reading, friends, music
  • ”be not solitary, be not idle”
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13
Q

Philippe Pinel and moral treatment

A
  • Philippe Pinel’s reform during French Revolution: Primary proponent in
    the movement for humanitarian treatment
  • Patients should be treated as sick human being rather than as beasts
  • Moral treatment: Emerged in later 18th century
  • Close contact with nursing staff/attendants
  • Staff would talk and read with them
  • Purposeful activities: residents should lead lives
    as close to normal as possible (within the
    constraints of their disorders)
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14
Q

Genetics: Francis Galton

A
  • Often considered the originator of genetic research
    with twins
  • Attributed behavioural characteristics to heredity
  • Coined the term “nature/nurture” (i.e. genetics vs environment)
  • Also ‘credited’ with creating the eugenics movement in 1883
    (Brooks, 2004).
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15
Q

Eugenics and Psychiatry

A

“Undesirable” characteristics should be eliminated in the population
by selective breeding.
* People with the “undesirable” characteristics should not have children.
* Forced sterilisation: By 1945, more than 45,000 people with
mental illness in the US were forcibly sterilised (Whitaker, 2002).
* Euthanasia: Killing of people with mental illnesses

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16
Q

Biological approaches of the 19th century

A

Blood letting: Treatment for agitated behaviour
* Hydrotherapy: Another treatment for agitated behaviour
* 33-36 oC
* Hours to days

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17
Q

Mesmer (1734 - 1815)and Charcot (1825 – 1893):

A

In the 18th century many people were observed to be affected by hysteria,
which referred to physical incapacities, such as blindness or paralysis, for
which no physical causes could be found.
* Both Mesmer and Charcot used a form of hypnosis to treat hysteria
(psychological approaches)

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18
Q

Josef Breur (1842-1945) ‘discovered’ the cathartic method

A

Cathartic method: “reprocessing” under hypnosis
* Reliving an earlier emotional trauma and releasing emotional tension by
expressing previously forgotten thoughts about the event
* Recalling the event associated with the first appearance of that symptom under hypnosis
and expressing the emotion felt at the time
* Influences on Freud

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19
Q

Franz Mesmer

A

Believed that hysteria was caused by a particular
distribution of a universal magnetic fluid in the body
(biological cause)
* Applied a method that reminded of hypnosis

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20
Q

Jean-Martin Charcot (1825-1893)

A

Although he thought that hysteria was a
problem with the nervous system (biological
cause), he was also persuaded by
psychological explanations
* Developed hypnosis
* Influence on Freud, Piaget, Binet

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21
Q

Libido

A

Libido (=the source of id’s energy): biological and
unconscious

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22
Q

Defense mechanisms

A
  • Un- or preconscious strategies used by the ego to protect
    itself from anxiety (such as repression and identification)
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23
Q

Freud and psychoanalysis

A

Psychoanalysis → psychodynamic treatments
* Still practiced today, although not as commonly as it once was
* The goal is understand the person’s early childhood experience, the nature of
key relationships, and the patterns in current relationships
* By making conscious what was repressed (e.g., the Oedipus Complex) it is
possible to overcome mental disorders

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24
Q

Free association and interpretation

A

Technique to help people explore their repressed and
unconscious conflicts
* Mostly talking about dreams which are interpreted by
the analyst
* Defence mechanisms are a principal focus of the interpretations

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Freud’s theory has evoked a lot of criticism during the last decades
Over-interpretation of the evidence generated during free association * Lack of empirical evidence for some assumptions * Existence of the three structures of the mind * Existence of the developmental stages such as the phallic stage * Existence of the Oedipus Complex * Lack of effectiveness of the technique of free associations in curing e.g., anxiety disorders → Psychoanalysis is no longer as influential as it once was
26
Extinction
When the CS is no longer followed by the UCS
27
Operant conditioning
Operant conditioning: B.F. Skinner distinguished two types of reinforcement: * Positive reinforcement: A response is strengthened by a pleasant effect * Negative reinforcement: A response is strengthened by removal of an aversive event, such as the cessation of electric shocks.
28
Modelling (social learning): Bandura
Learning often goes on in the absence of reinforcement * We all learn by watching and imitating others * Children of parents with phobias or substance abuse may acquire similar behaviour patterns, in part through observation
29
Systematic desensitisation and exposure therapy
Systematic desensitisation (Wolpe, 1958): A technique to treat phobias and anxiety. It includes two components * Deep muscle relaxation and * Gradual exposure in sensu (imagination) to a list of increasingly feared situation (starting with least unpleasant). * Exposure therapy in vivo (e.g., “Flooding”) or in virtual reality
30
Cognitive therapy
* Limitations of behaviourism: * Focusing only on behaviour and excluding cognition and emotion * Human beings do not just behave, they also think and feel * The importance of cognition * The way in which people think about, or appraise, situations can influence behaviour in a dramatic way * How people construe themselves and the world is a major determinant of psychological disorders * Helping clients to become more aware of their maladaptive way of thinking * Change feelings, behaviours, and symptoms by changing thoughts
31
Aaron Beck's Cognitive Theory
Based on a negative triad: negative view of the self, the world, and the future
32
Albert Ellis’s Rational-Emotive Therapy (Ellis, 1993, 1995)
Sustained emotional reactions are cause by internal sentences people repeat to themselves (self-statements such as “I am worthless”) * People with psychological distress maintain irrationally high demands towards themselves: concept of “demandingness” (Ellis, 1991) * Aim of the rational-emotive therapy is to eliminate these self-defeating beliefs and to reconsider irrationally high demands.
33
What mental disorders may serotonin and dopamine be involved with?
Depression, mania and schizophrenia
34
Norepinephrine
Produces high states of arousal and may be involved in anxiety disorders and other-stress related conditions
35
Agonist/Antagonist
A drug, that works on the neurotransmitter’s receptor to either stimulate or dampen the activity of that neurotransmitter
36
Second messenger
Released by the receptor, when a cell is firing more frequently * Helping a neuron adjust receptor sensitivity, when it has been overly active
37
5-HTT gene
Three variants: Short-short Short-long Long-long This gene is for serotonin transporter Caspi et al.’s study (2003): A large sample of children was followed from age 3 to age 26 * Assessment of the 5-HTT gene (SerotoninTransporter Polymorphism) and childhood maltreatment * People with the short-short allele combinations of the 5-HTT gene and who suffered maltreatment in childhood: → Increased risk of major depression
38
What is the neocortex?
Rational or thinking brain
39
What is the limbic brain?
Emotional or feeling brain
40
Reptillian brain
Instinctual or dinosaur brain
41
Prefrontal cortex
Involved in executive functions * Organising one’s behaviour (e.g., planning of behaviour, direction of attention, inhibition of dominant responses, working memory) * Poor executive functions are involved in most mental disorders * Prefrontal cortex helps to regulate the amygdala
42
Grey matter
The thin outer covering of the brain, consisting of neurons
43
White matter
Interior of the brain, large tracts of fibers that connect cortex with the spinal cord and other centers
44
What is part of the limbic system?
Hypothalamus Thalamus Amygdala Hippocampus
45
HPA Axis
Hypothalamus, pituitary gland and adrenal cortex Bi-directional relationship between the body and brain * Body actually feeds back to the brain * Diazepam (Valium) is used a muscle relaxant
46
Effects of cortisol
Adaptive: * Homeostasis – returns perturbed system back to normal * Allostasis – takes a system that is perturbed and adjusts the settings of the system so it is more appropriate to deal with the stressor * Maladaptive: * Allostatic load – sum of all adjustments to systems based on cortisol response
47
Autonomic Nervous System
* Sympathetic system; prepares the body for “fight or flight” * Parasympathetic system: helps the body to calm down * Operates very quickly, generally without our awareness
48
The neuroendocrine system - HPA-axis
HPA-axis (Hypothalamic-Pituitary-Adrenocortical axis) * Hypothalamus; releases corticotropin-releasing hormone (CRH), which communicate with the pituitary gland * Pituitary gland; releases adrenocorticotropic hormones, which travels via the blood to the adrenal glands * Adrenal cortex: releases cortisol (stress hormone) * Central to the body’s response to stress * Operates rather slowly: Reaction can be measured after around 10 minutes The autonomic nervous system: * Sympathetic system; prepares the body for “fight or flight” * Parasympathetic system: helps the body to calm down * Operates very quickly, generally without our awareness
49
How might cortisol damage the brain?
Sapolski and Pulsinelli (1985): * Cell loss in the hippocampus of rats * Implanted a placebo in one hemisphere (A) and a pellet of corticosterone in the other (B) * Bremner et al. (2000) - hippocampus 19% smaller in depressed individuals
50
Implications of hippocampal volume loss
* Hippocampus acts as a “break” on the HPA axis (Jacobson & Sapolsky, 1991) * Without hippocampus inhibition the system begins to break down * Sapolsky called this a “cascade” Untreated depression and hippocampal volume loss: * Sheline et al. (2003) found that longer untreated episodes were associated with reduced HC volume * Longer treated episodes were not associated with reduced HC volume * Antidepressants may protect against HC volume loss and be neuro-protective
51
Heritability
Extent to which variability of a trait or disorder can be accounted for by genetic factors * Estimates can range from 0.0 to 1.0 (these estimates are derived from similarities between identical versus fraternal twins or from adoption studies) * Caution: Estimates refer to the amount of variability of a certain trait which is due to genetic differences between individuals within the population (and not how much this trait is due to genetics within a particular individual)
52
Copy number variants
* Refers to an abnormal copy of one or more sections of DNA within the gene(s); addition/deletion cf. knockout studies * Identified in different disorders
53
Polymorphisms
Refers to a difference in DNA sequence on a gene that occurs in the population (at least 1%)
54
What sociocultural factors affect if people are more inclined to have a mental disorder?
Gender Socioeconomic status Cultural and ethnic factors Interpersonal factors - attachment theory The quality of relationships
55
Social exclusion
fMRI study shows that social exclusion activates the same part of the brain as physical pain does
56
Couples and family therapy
* Couples therapy * People in a distressed marriage are 2 to 3 times as likely to experience a psychological disorder (Whisman & Uebelacker, 2006) * Working with both partners to reduce relationship distress * Family therapy * Problems of the family impact on the members and vice versa * Family therapy often interprets specific symptoms of a family member as a problem of the family system
57
Depressive Disorders Symptoms
Cognitive symptoms * Self-recrimination, focused on deficits * Difficulty to concentrate * Physical symptoms * Fatigue and low energy * Sleep too much or too little, difficulty in fall asleep and night awakenings * Appetite/ weight loss or change in appetite * Decrease in sexual interest * Psychomotor retardation or agitation * Initiative disappears * Social withdrawal * Neglect of appearance
58
Major Depressive Disorder
* Diagnosis (DSM-5) of MDD * Symptoms: At least five symptoms of depression * Those must include either depressed mood or loss of interest/pleasure * Additional symptoms (cognitive, physical, initiative) * Time criterion: Symptoms must be present for at least two weeks * MDD is an episodic disorder * Present for a period and then clear * Recurrence * 2/3 of affected people experience at least one more episode (Solomon et al., 2000) * Mean: Four episodes (Judd, 1997) * With every new episode, the risk for further episodes increases by 16% (Solomon et al., 2000)
59
Dysthymia
* Chronic depressive disorder * Chronically depressed for more than half of the time and at least two additional symptoms * For at least two years (or one year for children/adolescents) * Mean duration: More than five years (Klein et al., 2006). * Symptoms * Do not clear for more than two months at a time * Are milder than with a MDD, but the disorder is not less severe because it is chronic
60
Epidemiology
Life-time prevalence (Kessler et al., 2005) * MDD ~ 16% * Dysthymia ~ 2.5% * Onset: Mostly in late teens to early twenties * Gender differences: After 15 MDD is twice as common as in women. * No gender differences in childhood (Nolen-Hoeksema & Girgus, 1991) * Increasing prevalence across the 20th century Socioeconomic status: * Prevalence three times higher when living in poverty * Poverty as a stressor
61
Bipolar
Termed “bipolar” * Because most people who experience mania, will also experience depression * An episode of depression is not required for bipolar I, but for bipolar II
62
Mania
* A state of intense elation or irritability. Related symptoms include that affected people may (get).. * Louder and make incessant stream of remarks * Flights of ideas * From sociable to intrusive * Excessively self-confident * Oblivious to the consequences of their behaviour (imprudent sexual activities, overspending, reckless driving) * Stop sleeping, but stay energetic * A manic episode lasts at least one week and causes significant distress or functional impairment
63
Hypomania
Less distinct symptoms * A hypomanic episode * Symptoms last at least 4 days * Clear changes in functioning, but no impairment * Does not cause serious problems * May feel more social, flirtatious, energised and productive * No psychotic symptoms
64
Bipolar I Disorder
* A manic episode at least once in a lifetime: * Distinctly elevated or irritable mood * Abnormally increased activity and energy * Time criterion: Over a week * Does not have to experience current symptoms (the episode may have been some time ago) * High rates of recurrence – more than 50% experience four or more episodes (Goodwin et al., 1990) * More severe form of mental illness than MDD * High rates of inability to work, of suicide, and of other medical conditions (Harrow et al., 1990)
65
Bipolar II Disorder
* To fulfil the diagnosis of Bipolar II Disorder: * At least one major depressive episode * At least one episode of hypomania * A milder form of bipolar disorder
66
Cyclothymic disorder
* A chronic disorder (similarly to dysthymia) * Symptoms last at least two years among adults (1 year in children and adolescents) * Frequent but mild symptoms of depression, alternating with mild symptoms of mania * The severity of symptoms is usually on a much lower level than in bipolar I/II disorder
67
Epidemiology of bipolar disorders
* Life-time Prevalence * Bipolar I disorder ~ 1% (Merikangas et al., 2011) * Bipolar II disorder ~ 0.4 – 2% (Merikangas et al., 2011) * Cyclothymia ~ 4% (Regeer et al., 2004) * Onset * In more than 50% before age 25 (Merikangas et al., 2011) * Gender * Equally often in women and men, but women experience more episodes (Altshuler et al., 2010) * Comorbidity * 2/3 also suffer from anxiety disorders * 1/3 also suffer from substance abuse (Harrow et al., 1990)
68
Lazarus and Folkman (1984)
One of the most popular psychological theories of stress * Transactional theory of stress * Describes the stages we go through when confronted with a potential stressor “Stress occurs when the situation is appraised as harmful and as exceeding our ability to cope Interpretation (appraisal) of the stressor is central to the theory – Person has control, not the environment!
69
Lazarus and Folkman (1984)
* Stress is seen as a transaction (an exchange) between the person and their environment * We tend to see stress as a one way thing – coming from the environment only * “My work is stressful” * “My car broke down, so I’m really stressed” * We proportion blame to the external environment, but in reality we have some control over whether something is stressful or not
70
Hans Selye - General Adaptation Syndrome
General Adaptation Syndrome (GAS): Three distinct physiological phases in reaction to chronic stress. * Alarm Reaction: A threat is perceived and the nervous system is triggered for survival * Stage of Resistance: The body tries to revert back to a state of homeostasis, trying to recover. The metabolic state of some organ tissues is higher (working overtime – state of arousal) * Stage of exhaustion: Organ tissues can no longer meet the demands placed upon them and they fail to function properly. Can result in the death of the organ and possibly death of the organism as a whole.
71
Diathesis-Stress Model
Psychopathology is much too diverse to be explained or treated by any one of the current paradigms * Links genetic, neurobiological, psychological, and environmental factors * Model: Interaction between diathesis and stress o Diathesis: predisposition towards disease o Stress: environmental or life disturbances o Both are necessary to develop a disorder * Diathesis increases the risk, but does not guarantee development of a disorder * Stress is necessary in order that the diathesis is translated into an actual disorder
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Genetic factors - Bipolar and MDD
* Heritability of depression/bipolar disorder: Twin studies reveal a heritability of… o 37% for MDD o 93% for bipolar disorders (Kieseppa, Partonen, Haukka et al., 2004) * Specific genes/regions: o Inconsistent results, often non-replications (Segurado et al., 2003) o Probably it is rather a set of genes than a single gene
73
Genes related to mood disorders
* However, two polymorphisms have more consistently been related to vulnerability to develop MDD: o Polymorphism of the serotonin transporter gene (5-HTT) * Influence on serotonin function (Caspi et al., 2003) o Polymorphism of the DRD4.2 gene * Influence on dopamine function (Lopez Leon et al., 2005) * Genes may guide the way people regulate emotions or respond to life stressors (Kender et al., 2006)
74
Serotonin
- Most common antidepressant medications (SSRI) target serotonin system - Serotonin transporter polymorphism (5-HTT) interacts with environmental adversity to increase risk of depression.
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Dopamine
Plays a major role in the sensitivity of the reward system (→ pleasure, motivation, energy) - Diminished function: deficit in pleasure, motivation and energy in depression - Increased function: Joy, goal-driven behavior, energy in mania
76
Antidepressants
o Antidepressants rapidly change the neurotransmitter levels, the effect on the symptoms occurs with a lag of around 2 weeks (sometimes even a transient worsening of symptoms has been reported within the first few days) o metabolites of serotonin are not different in people with MDD in terms of absolute levels (Placidi et al., 2001; Ressler& Nemeroff, 1999)
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Sensitivity to receptors
* Sensitivity of serotonin receptors o people with insensitive receptors experience depressive symptoms as levels of serotonin drop * Studies with tryptophan the major precursor of serotonin o depletion of tryptophan causes temporary depressive symptoms among people with a history of depression/ family history o depletion of tryptophan causes no depressive symptoms among people without any history of depression/ family history (Benkelfat, Ellenbogen, Dean, et al.,1994; Neumeister, Konstantinidis, Nicholson, et al., 2002) → People who are vulnerable to depression may have less sensitive serotonin receptors (Sobczak, Honig, Nicholson, et al., 2002)
78
Four primary brain structures that have been studied the most in depression:
o the amygdala (Elevated level in depression and in mania) o the hippocampus (DIminished level in both depression and maina) o the subgenual anterior cingulate (Elevated level in depression and mania) o the dorsolateral prefrontal cortex (Diminished level in both depression and mania) o Striatium (Diminished level in depression and elevated level in mania)
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Amygdala
Elevated activity of the amygdala among people with MDD − upon presentation of negative words/pictures (threatening stimuli); people with MDD have a more intense and sustained reaction (Sheline et al., 2001) * One “theory“: − overactivity in the amygdala during depression causes oversensitivity to emotionally relevant stimuli − Diminished response to positive feedback may explain why people with depression are less motivated by positive events in their lives. − systems involved in regulating emotions are compromised (subgenual anterior cingulate, the hippocampus, and the dorsolateral prefrontal cortex)
80
Other brain structures in depression
Furthermore MDD is associated with structures that are important for emotion regulation (Phillips et al., 2008a): * greater activation of the subgenual anterior cingulate (Gotlib & Hamilton, 2008) o a decrease of activity relieves depressive symptoms (Mayberg, Lozano, Voorn et al., 2005) * diminished activation of the hippocampus during exposure to emotional stimuli (Davidson et al., 2002; Schaefer et al., 2006) * diminished activation of the dorsolateral prefrontal cortex when asked to regulate emotions (Fales et al., 2008)
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Striatum
Striatum: Nucleus accumbens: central component of reward system motivation to pursue rewards → Diminished activity to rewarding stimuli in depression → Elevated orientation to reward stimuli in bipolar disorder (Chen et al., 2011)
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HPA-Axis - cortisol dysregulation
* The Hypothalamic-PituitaryAdrenocortical–Axis (HPA-Axis): o the biological system that regulates reactivity to stress o may be overly active during episodes of MDD o triggers the release of cortisol (main stress hormone) o cortisol increases activity of the immune system
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Various findings link depression to high cortisol levels
o Among people who are depressed, cortisol levels are often higher than in people who are not depressed o The HPA-axis does not seem to respond well to biological signals to decrease cortisol levels in MDD (Garbutt et al., 1994) o Cushing‘s syndrome: causes oversecretion of cortisol, let people experience depressive symptoms o animal studies: chemicals that trigger cortisol release produce many of the classic symptoms (Gutman et al., 2003)
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Social factors
* The role of stressful life events o in triggering episodes of depression o neurobiological theories are consistent with increased reactivity to life events among people with MDD * Expressed Emotion o family member‘s critical or hostile comments toward the person with depression o High expressed emotion strongly predicts relapse in depression (Butzlaff et al., 1998) * Reciprocal causality between social factors and MDD o interpersonal problems can trigger depression, but.. o once depressive symptoms emerged, they can also increase interpersonal problems such as negative reactions from others (Coyne, 1976)
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Adverse Childhood Experiences
Adverse Childhood Experiences (ACE) Scale * ACE score = number of categories reported: o Emotional abuse o Physical abuse o Sexual abuse o Household substance abuse o Household mental illness o Mother treated violently o Incarcerated household member o Parental separation Higher the ACE score higher the percentage with a history of depression
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Beck's Theory
* Beck‘s theory, negative triad: negative views of the self, the world, and the future * Hopelessness theory: hopelessness as an important trigger of depression two key dimension of attributional style: − expectation that a desirable outcome will not occur − expectation that one has no skills available to change this situation (Lack of control)
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Rumination theory
o tendency to ruminate (dwelling on sad thoughts) increases the risk of depression (Nolen-Hoeksema, 1991) o Lack of executive control that might stop rumination and regulate the focus of attention
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Cognitive therapy
* Based on the idea that depression is caused by negative schemas & cognitive biases, such as the Beck’s negative triad (negative views of the self, the world, and the future) * The aim of cognitive therapy is altering maladaptive thought patterns − to identify thought patterns that contribute to depression − to learn how to challenge negative beliefs − to learn strategies that promote making realistic & and positive assumptions * Cognitive therapy is efficient in relieving symptoms of MDD
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Mindfulness-based cognitive therapy
* Adaptation of Cognitive Therapy o Focuses of relapse prevention (Segal et al., 2001) * The goal of MBCT is altering maladaptive thought patterns − to teach people to recognize when they start to become depressed − to try to adopt a “decentered” perspective − (negative) thoughts as merely “mental events”, not core aspects of the self * Meta-analyses show that MBCT is efficient in the treatment of MDD, as effective as CBT
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Behavioural activation therapy
* Based on the idea that depression is caused by a lack of positive experiences (→ low levels of positive reinforcement) * The goal of Behavioral activation therapy is to increase participation in positively reinforcing activities (Martell et al., 2001) * Behavioral activation therapy relieved symptoms of MDD and prevented relapse over a 2-year follow- up period (Teasdale et al., 2000) * Large “non-inferiority trial” in the UK showed that Behavioral activation alone works as well as Cognitive Behavioral Therapy for Depression; Behavioral activation seems to be the most effective and efficient “ingredient” of CBT (Richards et al., 2016, Lancet)
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Interpersonal therapy
* Based on the idea that depression is caused by interpersonal problems (Klerman et al., 1984) * The goal of Interpersonal therapy is to identify major interpersonal problems and trying to find solutions (in a one-toone therapy setting). These interpersonal problems may include: o role transition o interpersonal conflicts o bereavement o interpersonal isolation * Interpersonal therapy appears to be helpful in relieving depression and dysthymia (Elkin et al., 1989; Markowitz, 1994)
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Behavioural couples therapy
* Based on the idea that depression is caused by relationship problems * Behavioral couples therapy works with both members of a couple to improve communication and relationship satisfaction (Jacobson et al., 1991) * Behavioral couples therapy is as effective as individual cognitive therapy when a person with depression is also experiencing marital distress
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Biological treatment of mood disorders
Medication for mood disorders * Electroconvulsive therapy for depression
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Medication for depressive disorders
* drugs are the most commonly used and best-researched treatment for depression * 50-70% of people show major improvement * there are three major categories of antidepressants, that show all the same effectiveness (Depression Guideline Panel, 1993) − monoamine oxidase inhibitors (MAOI’s) − Block an enzyme known as monoamine oxidase which break downs and removes norepinephrine − tricyclic antidepressants − Inhibits the recycling of neuroepinephrine − selective serotonin reuptake inhibitors (SSRI) − Prevent or slow the reabsorption of serotonin in the brain
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Is there an overestimation of effectiveness of antidepressants? (Turner et al., 2008)
− only 51% of all studies were rated as having positive findings − less than half of the studies with negative findings were published and even in those the findings were described as positive * Antidepressants work better for some people than for others - they work best for individuals with very severe depressive symptoms (Kirsch et al., 2008) * There is a strong placebo response in studies on antidepressants (Kirsch et al., 2008)
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STAR-D trial (Rush et al., 2006)
− included 3671 patients, not excluding people with comorbid disorders − if they did not respond to the first SSRI, they were offered a choice of different medications to add or cognitive therapy − findings were sobering, only about 1/3 of patients achieved full symptom relief when treated with the SSRI − high rates of relapse, only 43% achieved sustained recovery (Nelson, 2006)
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Electroconvulsive therapy
* the most dramatic and controversial therapy * ECT is only used to treat people with MDD, that have not responded to medication * passing a 70-130-volt current through the patient’s brain (McCall et al., 2000) * ECT is more powerful than antidepressants with a 90% response rate (Pagnin et al., 2004) * risk of short-term confusion and memory loss
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Treatments for Bipolar Disorder
* Mood stabilisers: Help control manic and depressive episodes e.g., lithium * Typically lithium + other medications (e.g., Depakote or Olanzapine) o Like lithium these medications help reduce mania and, to some extent, depression * Anti-depressants can be prescribed if depressive symptoms persist but not generally recommended o Firstly, because it is not clear whether antidepressants help reduce depression when already taking a mood stabilizer o Secondly, studies show that antidepressants could be linked to a modest increase in the risk of a manic episode if taken without a mood stabiliser (Pacchiarotti et al., 2013) * Psychological treatments can supplement medication o To understand the disorder and treatments, avoid symptom triggers, and to recover from the social and psychological problems caused by the episodes. * Includes psychoeducation, cognitive therapy, family-focused therapy, interpersonal therapy. o All seem to improve depressive symptoms o However, no concrete evidence that one therapy is better than others
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Schizophrenia
* A group of disorders (not only one) characterised by disorganised thinking and disturbed emotions/perceptions
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What percentage of the population are affected by schizophrenia?
Affects 1-2% of worldwide population
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Symptoms of schizophrenia
Symptoms: * 1) Bizarre delusions: Paranoid and delusions of grandeur (i.e. high rank or of social importance) * 2) Hallucinations: Auditory, visual and tactile * 3) Incoherent, loose word associations * 4) Abstraction – concreteness of thought * 5) Severe emotional abnormalities * 6) Withdrawal into inner world (asociality) * 7) Alogia – significant reduction in the amount of speech * 8) Avolition – diminished motivation / interest / persistence in everyday routine and social activities * 9) Anhedonia – loss of pleasure (consummatory vs anticipatory) * 10) Some patients can find themselves in a “catatonic” state
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What is abstraction?
Concreteness of thought
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What is Alogia?
Significant reduction in the amount of speech
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What is avolition?
Diminished motivation / interest / persistence in everyday routine and social activities
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What are positive symptoms of schizophrenia?
Delusions and hallucinations
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What are negative symptoms of schizophrenia?
Avolition, alogia, anhedonia, blunted affect, asociality
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What are disorganised symptoms of schizophrenia?
Disorganised behaviour, disorganised speech
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Anosognosia
A symptom of severe mental illness experienced by some that impairs a person’s ability to understand and perceive his or her illness * “I’m not sick, I don’t need help” * Many people stop taking their medications due to this * This is not resistance, laziness or stubbornness
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Delusions
* A delusion is a fixed, false belief held despite what everyone else believes and obvious evidence to the contrary * Schizophrenics struggle to accept it’s not true * Never confront – causes conflict * Symptoms are often a self-protective, albeit maladaptive coping strategy (e.g. withdrawal) * Trying to make sense of things – if people are out to get me I shouldn’t engage with them, I should avoid them and protect myself * What about positive voices? Don’t want them to go away
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First expression of schizophrenia
* Usually seen between age 15 and 30 * Occurs during cortical pruning process * First signs include insensitivity to others, social isolation and anxiety, poor peer relationship, emotional lability, behaviour problems in boys, difficulty concentrating * Later signs include flat affect, odd behaviour, magical thinking and unusual perceptions * Causes progressive damage during the first few years (autotoxicity) * Severity of damage can be lessened with appropriate and early intervention * May sometimes be preventable – if we spot the early signs then incidence can be reduced
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Which artist painted cats and had schizophrenia?
Louis Wain
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History of schizophrenia
* Historical development of the concept and the DSM-5 criteria for diagnosis * Emil Kraepelin (1856-1926) referred to “dementia praecox” (dementia of early life) * Paul Eugen Bleuler (1857-1939): “schizophrenia” was coined in 1910, and is derived from the Greek words ‘schizein’ (split) and ‘phren’ (mind).
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DSM-5 Criteria for Schizophrenia
1. For 1 month, individual displays two or more of the following symptoms much of the time: a) Delusions b) Hallucinations c) Disorganised speech d) Very abnormal motor activity and disorganised (catatonic) behaviour e) Negative symptoms (diminished motivation or emotional expression) 2. At least one of the individual’s symptoms must be a, b, or c. 3. Functioning in work, relationships, or self-care has declined since onset and is much more reduced in various life spheres than was the case prior to the symptoms. 4. Beyond this 1 month of intense symptomatology, individual continues to display some degree of impaired functioning and signs of disorder for at least 5 additional months.
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Brief psychotic disorder
Various psychotic symptoms such as hallucinations, delusions, disorganised speech, restricted or inappropriate affect, and catatonia * Symptom duration of less than 1 month
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Schizophreniform Disorder
* Various psychotic symptoms such as hallucinations, delusions, disorganised speech, restricted or inappropriate affect, and catatonia * Symptom duration of greater than 1 month but less than 6 months
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Schizoaffective Disorder
* Marked symptoms of both schizophrenia and a major depressive episode or a manic episode * Symptom duration of 6 months or more
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Delusional Disorder
Persistent delusions that are not due to schizophrenia * No other symptoms of schizophrenia * Symptom duration of 1 month or more
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Core brain areas in schizophrenia
* Frontal areas * Temporal lobes * Basal ganglia * Limbic system
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Functional impairment in Schizophrenia
Hypofrontality in the frontal areas People with SZ cannot do complex working memory tasks e.g hear letters and say different ones to those you heard
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Temporal lobes in schizophrenia
* “The reality checker” – has many dopamine pathways * Perception (hallucination) * Reality orientation (delusion) * Memory * Temporal (perceives) - - - - - - - - - - - - - - - - - > Frontal (processes) * No schizophrenia: * Hearing speech →Temporal sends to the frontal lobe to makes sense of it * Thinking → Frontal lobe only * Schizophrenia: * Hearing speech →Temporal sends to the frontal lobe to makes sense of it * Hearing voices → Temporal lobe is activated + frontal lobe to make sense of it
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Basal Ganglia in Schizophrenia
Basal Ganglia * “The Filter” * Filters out irrelevant sensory input * Regulate arousal * Govern concentration Schizophrenics usually have lower basal ganglia activity
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Limbic system and SZ
Limbic system * Understanding emotional events * Linking current perceptions to past memories * Learning from experience * Structural damage in schizophrenia
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History of Treatments - Schizophrenia
Since the physiopathology of schizophrenia was completely unknown, all therapeutic efforts in 1930s-1940s were launched on an almost random trial-and-error basis. Fever therapy Deep sleep therapy Gas therapy Insulin shot therapy Electroconvulsive or electroshock treatment Lobotomy
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Biogenic amines
Biogenic amines: Catecholamines Norepinephrine Epinephrine Dopamine Histamine Serotonin
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Dopamine hypothesis
Agonist (Amphetamine) promotes the release of dopamine and fosters symptoms of schizophrenia Agonist - both amphetamine and cocaine block reuptake of dopamine and foster symptoms of schizophrenia Antagonist (Chlorpromazine) a drug that blocks symptoms of schizophrenia occupies the dopamine site on the D2 receptor preventing receptor activation by dopamine
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Chlopromazine - treatment of schizophrenia
Henri Laborit (1950) was looking for drugs to relax patients prior to surgery and tried various anti-histamines He found Chlorpromazine effective It was so effective in calming patients that he thought it might work on calming schizophrenic patients It was spectacularly successful and only later was it known to block dopamine
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Dopamine Hypothesis and Chlorpromazine
Chlorpromazine was the first effective neuroleptic drug Antipsychotic drugs like chlorpromazine block DA receptors Long term usage of phenothiazines often develops Parkinsonian-like symptoms (tardive dyskinesia) Generally, first generation drugs for treating schizophrenia only reduce positive symptoms Amphetamine psychosis resembles schizophrenia Amphetamine blocks DA transporters, thereby raising DA levels Amphetamine exacerbates schizophrenia
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Neurotransmitters involved in Schizophrenia
Serotonin similar to the chemical structure of major hallucinogens LSD Psilocybin Glutamate: Phencyclidine (PCP) also known as angel dust acts on glutamate receptors and leads to hallucinations
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Second-generation antipsychotics
Clozapine/Clozaril – works by balancing levels of dopamine and serotonin in the brain. Fewer motor side effects Less treatment noncompliance Reduces relapse Reduces positive and disorganised symptoms, modestly more effect than the 1st generation drugs in reducing negative symptoms Some evidence shows the new medicines may improve cognitive function.
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Side effects of chlorpromazine
First generation: Movement disorders, cardiovascular issues Second generation: Metabolic syndrome, cardiovascular issues, weight gain, changes to blood sugar levels Other common side effects: Sedation, sexual dysfunction, constipation, agitation, dizziness, suicidal thoughts and behaviours. Close monitoring advised
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Heritability of schizophrenia
If a disease is inherited, then family member of a diseased patient should be at higher risk The risk should increase with closer ties Twin studies: Identical (monozygotic) twins have same genes whereas fraternal (dizygotic) twins share 50% of their genes If both twins carry the disease they are concordant If only one twin carries it they are discordant The rate of concordance in identical twins is an important indicator of heritability
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Heritability of schizophrenia
Suggests a strong genetic component to schizophrenia Note that even identical twins are not 100% concordant i.e. genetics are not the whole story MRI Images of monozygotic twins discordant for schizophrenia Ventricles are enlarged: Cortical compression in schizophrenia
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Genes associated with SZ
BDNF – Brain-derived neurotrophic factor is critical for the survival of central nervous system COMT – Associated with executive functions that rely on the prefrontal cortex SNPs analysis: In schizophrenia Major histocompatibility complex genes (MHC) The MHC is a set of cell surface proteins essential for the immune system to recognise foreign molecules, which in turn determines histocompatibility DISC1: Disrupted in Schizophrenia Possibly associated with dopamine impairments
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Is schizophrenia a disorder of language?
FoxP2 – First discovered in a family with a rare severe speech and language disorder Take out in mice there’s less vocalisation and simpler vocalisation. Add in human version and there’s more vocalisations and more complex ones. Li et.al (2013) focused on 12 SNPs in the FoxP2 gene 1135 schizophrenia patients, 1135 unrelated major depression patients, 1135 unrelated bipolar patients, 1135 unrelated controls FoxP2 is significantly associated with schizophrenia and major depression
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Demographics - SZ
Age: Late adolescence/early adulthood onset Often in response to a major stressor/crisis (43% of cases have significantly greater recent life stressors than healthy controls) Frontal cortex: Maturation up until 25 y.o. Elderly: Positive symptoms disappear, negative symptomology increases Gender: Affects men slightly more than women Usually appears a little earlier in men than women Socioeconomic status: Sociogenic theory Social drift theory Research supports social drift theory Cultural differences: Schizophrenia is a disease of abnormal thought but what counts as not normal is hugely impacted by cultural norms Prevalence in migrants is higher compared to native-born individuals (could be bias in diagnostic practices, exposure to greater stress, less access to treatment, etc.)
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Parenting styles and SZ
Leading psychiatric journals in the 1950s published many articles claiming that abnormal parenting is the cause of schizophrenia “Schizophrenogenic mothering style” Conflicting emotional messages Distorted and conflicting demands from the mother leads to schizophrenia This is not the case at all
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Family factors
The family does not seem to have an impact on the origin (cause) of the disorder, but they can have an impact on recovery. Expressed Emotion (EE): Particular emotions, attitudes and behaviours expressed by relatives towards a family member diagnosed with SZ – hostility, critical comments, emotional overinvolvement, overprotectiveness. Research shows: > 70% of patients in high EE families relapsed within a year follow up, compared to 31% of patients in low EE families 58% of people returning to high EE homes had gone back to the hospital, compared to 10% of people returning to low EE homes
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Prenatal stress and SZ
Evidence: Rats: expose them prenatally to loads of glucocorticoids = elevated dopamine levels in the frontal cortex Foetus during famine in china (1959-1961) = higher than expected rate of schizophrenia Foetus during Dutch Hunger Winter (1944-45) = higher than expected rate of schizophrenia Birth trauma = higher than expected rate of schizophrenia Mothers exposed to infections (e.g. viruses) such as the flu in second trimester of pregnancy = higher risk of schizophrenia A pathogenic challenge to the system – a pathogenic stressor Perinatal hypoxia: Oxygen deprivation at birth or in the few weeks before or after birth. Toxoplasma: A protozoa parasite which is released in the faeces of cats Increased risk of schizophrenia
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Individuals at high risk for psychosis
Van der Steen et al. (2017): Clinical high risk for psychosis: the association between momentary stress, affective and psychotic symptoms CHR individuals are more sensitive to daily life stressors than psychotic patients Thus, stress sensitization seems to play a role particularly in the early phase of psychosis development i.e. stress sensitization occurs prior to the development of a full blown psychotic state
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Treatment - SZ
Patient Outcomes Research Team (PORT) treatment recommendation: Medication plus psychosocial intervention Family therapy Cognitive behavioural therapy Social skills training
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Financial and societal costs of SZ
Schizophrenia and psychosis cost the UK health budget £11.8 billion Secure care costs £1.2 billion or 19% of the mental health budget each year. Only 8% of people with schizophrenia are in employment People with schizophrenia and psychosis die on average 10-20 years younger than the general population
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Research challenges of SZ
Psychotic episodes – fluctuations in symptoms Mood instability: Different stages of the illness and alleviation of symptoms Medication use and mis-use Drug taking and/or alcohol
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An evolutionary perspective on SZ
An evolutionary perspective: Darwin – adaptation and survival of the fittest Schizophrenics procreate at lower rates than the general population Schizophrenia appears to be maladaptive and so it’s not clear why it would be selected for… However … Some talk/evidence of anti-cancer properties (e.g., lung, throat)
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Emil Kraepelin
Kraepelin classified what was previously considered to be a unitary concept of psychosis, into two distinct forms of: Manic depression (now seen as comprising a range of mood disorders such as recurrent major depression and bipolar disorder), and Dementia praecox (nowadays known as schizophrenia). Kraepelin believed dementia praecox has a biological cause (i.e., anatomical or toxic processes cause the disease) and results in progressive inevitable intellectual deterioration. Identified that the disease had an early onset His work played a role in the thinking behind current classification systems and categorisation of mental health disorders:
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Anxiety
Anxiety: an apprehension over an anticipated problem – about a future threat (e.g. concern about the possibility of unemployment) – Helps planning for future threats, improves preparedness – Involves moderate arousal
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Fear
Fear: a reaction to immediate danger – a threat that’s happening now (e.g. facing a bear) → rapid changes in sympathetic nervous system – Involves higher arousal
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Clinical description of anxiety disorders
* All anxiety disorders share excessively high or frequent anxiety * They also involve tendencies to experience unusually intense fear (except for generalized anxiety disorder) (Cox et al., 2002) – Symptoms must interfere with important areas of functioning and/or cause distress – Symptoms are not caused by a drug or a medical condition – Symptoms persist for at least 6 months, or at least 1 month for panic disorder. * Each disorder is defined by a distinct set of symptoms related to anxiety or fear. However, there is also some overlap in the way the various anxiety disorders are defined
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Clinical descriptions of anxiety disorders
Specific phobia - Fear of objects or situations that is out of proportion to any real danger Social anxiety disorder - Fear of unfamiliar people or social scrutiny Panic disorder - Anxiety about recurrent panic attacks Agoraphobia - Anxiety about being in places where escaping or getting help would be difficult if anxiety symptoms occurred GAD - Uncontrollable worry
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Specific phobias - Diagnostic criteria
Diagnostic criteria * Fear of objects or situations that is out of proportion to any real danger * The object or situation is avoided or else endured with intense anxiety * The symptoms persist for at least six months – The person recognizes that the fear is excessive (→ in DSM 5 this is not any more a criterion) – High comorbidity among specific phobias (Kendler et al., 2001)
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SAD - diagnostic criteria
Diagnostic criteria * Fear of unfamiliar people or social scrutiny * Trigger situations are avoided or else endured with intense anxiety * The symptoms persist for at least six months – The most common fears include public speaking, meeting new people, and talking to people in authority (Ruscio et al., 2008) – It normally begins during adolescence when social interactions become more important – It can range from a relatively few specific fears to a more generalized host of fears (Acaturk et al., 2008)
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Panic disorder - Diagnostic criteria
* Recurrent unexpected panic attacks, unrelated to specific situations * At least 1 month of concern about the possibility of more attacks, their consequences, or maladaptive behavioral changes because of the attacks * Panic attack: − a sudden attack of intense apprehension, terror, and feelings of impending doom (cf. fear like when faced with an immediate threat) − accompanied by at least four other symptoms (e.g. physical symptoms including shortness of breath, heart palpitations etc., depersonalization, derealization, fears of losing control) − the symptoms tend to come on very rapidly and reach a peak within 10 minutes – The onset is typically during adolescence – Lifetime prevalence: 6%
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Agoraphobia - diagnostic criteria
* Disproportionate and marked fear or anxiety about at least two situations where it would be difficult to escape or receive help * Situations are avoided or are endured with intense fear or anxiety * Symptoms last at least six months – It is suggested that half of the people with agoraphobia do not have panic attacks (Wittchen et al., 2008) – But they are concerned about what will happen if other anxiety symptoms develop – Agoraphobia is related to significant impairment in daily functioning (Wittchen et al., 2010)
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GAD - diagnostic criteria
* Excessive anxiety and worry at least 50% of days about a number of events * The person finds it hard to control the worry * The anxiety or worry is associated with at least three physical symptoms (cf. restlessness, easily fatigued, muscle tension, sleep disturbance, difficulty concentrating) * Symptoms last at least six months – Patients worry about general issues such as relationships, health, finances, and daily hassles- but much more than would be considered adequate and this interferes with daily life (Roemer et al., 1997) – It typically begins in adolescence, and is often chronic
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Comorbidity in anxiety disorders
More than half of people with one anxiety disorder meet the criteria for another anxiety disorder (Brown et al., 2001) * But there is also a high comorbidity with other disorders; 75% have at least one other psychological disorder (Kessler et al., 1997) – About 60% also meet the diagnostic criteria for depression (Brown et al., 2001) – Comorbidity also with substance abuse and personality disorders (Jacobson et al., 2001; Johnson et al., 1992) – Comorbidity is associated with poorer outcomes (Newman et al, 1998).
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Risk factors in anxiety disorders
Gender: women are twice as likely as men to be diagnosed (de Graaf et al., 2002) – women may be more likely to report their symptoms – men may believe more in their personal control over situations (protective) – gender roles: men may experience more social pressure to face fears – women may experience different life circumstances
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Culture and anxiety disorders
People in every culture experience problems with anxiety disorders Cultures with recent war, revolution, large-scale prosectution or poverty have higher levels of anxiety disorders Culture and environment influence what people fear Examples: Kayak-angst (inuit, western Greenland) - fear of going out on boats alone Taijin kyofusho (Japan) - fear of body odour or blushing Koro (southern and eastern Asia) - worry about the genitals going up into the body Susto (Latin America)
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Behavioural theory involving Fear conditioning: Mowrer’s (1947) two factor model of anxiety disorders
1. Classical conditioning: a person learns to fear a neutral stimulus (CS) that is paired with an intrinsically aversive stimulus (UCS) (→ fear develops) 2. Operant conditioning: a person gains relief by avoiding the CS (→ fear does not go extinct, as one avoids the CS; perpetuating factor)
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Criticism regarding Mowrer’s two factor model
It is rarely clear that classical conditioning has occurred by direct experience * Many people with anxiety disorders do not remember a specific incident; many people who experience threats do not develop anxiety Ways how anxiety/fear might develop: 1. direct experience (e.g. conditioned fear of dogs; just as in Mowrer’s Model) 2. observation of another person harmed or frightened by a stimulus (modeling). 3. verbal instruction (for example by a parent warning a child that dogs are dangerous) or even thoughts (→ cognitive factors)
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Some people seem to acquire fears more readily (e.g. through classical conditioning) and to show a slower extinction of fears once they are acquired (Craske et al., 2009).
Study by Michael et al. (2007) * Classical conditioning: Pairing a neutral picture with electric shock → people with and without anxiety disorders developed conditioned fear response * Extinction phase (picture without the shock) → people without anxiety disorders showed a drop in their fear response, people with panic disorders showed very little decrease in fear response
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People with anxiety disorders are particularly sensitive to unpredictable threats (Gorka et al., 2017)
Neutral predictable unpredictable (NPU) threat task: * Neutral condition: no aversive stimulus * Predictable condition: aversive stimulus is preceded by a warning * Unpredictable condition: aversive stimulus without warning → People with social anxiety disorders, specific phobias, panic disorders and PTSD show particularly high psychophysiological arousal in the unpredictable condition compared to controls → People with MDD respond like controls
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Risk factors across anxiety disorders - Genetic
* some gene variants may elevate the risk for anxiety disorders * Large-scale twin study: heritability estimate of .5 to .6 (Kendler et al., 2011) → genes may explain 50 to 60% of the risk for anxiety disorders in the population * Having a family member with phobia is related to increased risk of developing not only phobia, but other anxiety disorders (Tambs et al., 2009) → related to genes for neuroticism?
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Anxiety - neurobiological factors
Neurobiological factors: The fear circuit * Elevated activity in the amygdala (greater response to angry faces) among people with anxiety disorders * Hippocampus: encoding the context in which feared stimuli occur * Less activity in the medial prefrontal cortex: – regulates the amygdala – involved in extinction of fears – Regulates emotions: conscious processing of fear and anxiety Neurobiological factors: Activity of neurotransmitters * Disruption in serotonin levels in people with anxiety disorders (Frick et al., 2015) * Changes in the function of the GABA system (Bandelow et al., 2016) * GABA involved in modulating the activity in the amygdala and fear circuit * Increased levels of norepinephrine and changes in the sensitivity to norepinephrine receptors (Neumeister et al., 2005) – Norepinephrine involved in the activation of the fight-or-flight response
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Risk factors across anxiety disorders - personality
Personality factors * Behavioural inhibition in infants: tendency to become agitated and cry when faced with novel stimuli * 45% of infants with elevated behavioural inhibition showed symptoms of anxiety at age 7.5 years vs. 15% of infants with low behavioural inhibition (Kagan & Snidman, 1999) * Neuroticism: tendency to experience frequent or intense negative affect – Neuroticism predicts onset of anxiety disorders and depression (Ormel et al., 2013) – People with high levels of neuroticism are more than twice as likely to develop an anxiety disorder (de Graaf et al., 2002)
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Risk factors across anxiety disorders - cognitive factors
* Sustained negative beliefs about the future: believing that bad things are very likely to happen – patients engage in safety behaviours to sustain their negative beliefs and thereby corroborate the negative beliefs – For example, people who fear they will die from a heart attack will stop all physical activity once they feel their heart race. * Perceived lack of control: degree to which a person experience control over their environment – Aversive and traumatic experiences may promote a view that life is not controllable * Attention to Threat: Increased attention to negative cues in the environment (Williams et al., 1997) – E.g., people with social anxiety selectively attend to negative faces; people with snake phobias selectively attend to cues related to snakes – Once a threatening stimulus has captured attention, anxious people have difficulty diverting their attention away from the object. * Intolerance of uncertainty: difficulty with accepting ambiguity and an uncertain future: – More likely in people with anxiety disorders
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Prepared learning
* Only certain kinds of stimuli contribute to the development of a phobia (snakes, spiders vs. flowers, lambs) * During human evolution, people learned to react strongly to stimuli that could be life-threatening (Seligman, 1971) →Evolution might have prepared our fear circuit to learn fear of certain stimuli quickly and automatically →Even infants and monkeys are more likely to be conditioned to fear such life-threatening stimuli (Cook & Mineka, 1989) * Initially, people can be conditioned to fear many types of stimuli, but fear of naturally dangerous stimuli is sustained (Dawson et al., 1986; McNally, 1987).
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Mowrer’s behavioural two-factor model:
* Classical conditioning: negative social experience (direct, through modelling, verbal instruction) * Operant conditioning: Avoidance of social situations acts as reinforcement → conditioned fear cannot be extinguished * Safety behaviours/avoidant behaviours (avoiding eye contact, disengaging from conversation, standing apart) → Others tend to disapprove of these behaviours which intensified the problem
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Model of the development of Social Anxiety Disorder
* Unrealistically harsh views of their social behavior and overly negative belief about the consequences of their social behavior * Focus their attention on how they perform in social situations and rather than their interaction partner * Attend more to internal cues (do I feel anxious?) than external social cues (what is the other person trying to say?) → Avoidance of social situations, increased anxiety
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Model of the development of panic disorder
* a panic attack involves activation of the sympathetic nervous system * Locus coeruleus: Major source of norepinephrine → surges in norepinephrine as a natural response to stress; support of fight-or-flight response * People with panic disorder show a more dramatic response to drugs that trigger release of norepinephrine (Neumeister et al., 2005) Behavioural factors: Classical conditioning * Interoceptive conditioning: Panic attacks are often triggered by internal bodily sensations of arousal (e.g., increased heart rate)
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Model of the development of panic disorder: Cognitive factors
* catastrophic misinterpretation of these somatic changes (Clark, 1997) * e.g. the person interprets bodily sensation, such as an increase of heart rate, as a sign of an impending heart attack * Inter-individual difference (e.g., Anxiety Sensitivity Index; Telch et al., 1989)
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Model of the development of agoraphobia
Only recognized as a distinct disorder in the DSM-5 (not as much much research so far…) Cognitive factors: Fear-of-fear hypothesis (Goldstein & Chambless, 1978): * Agoraphobia is driven by negative thoughts about the consequences of experiencing anxiety in public * Catastrophic beliefs that anxiety might lead to unacceptable consequences. * Behavioural factors: Conditioning – successfully avoiding social situation may reinforce behaviour
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Model of the development of Generalised Anxiety Disorder (GAD)
* High comorbidity with other anxiety disorders → general factors predicting anxiety disorders important * High comorbidity with MDD → risk factors involved in MDD Worry: Core feature of GAD * Negative affect, modest psychophysiological arousal, distress Contrast avoidance model (Newman & Llera, 2011): * People with GAD are aversive to experiencing rapid shifts in emotion. * Prefer to sustain a chronic state of worry and distress instead → stable emotional state (but an unpleasant one)
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Locus Coeruleus
* Sometimes referred to as the adrenal gland in the brain * 40,000 norepinephrine cell bodies Excitatory neurotransmitters: Glutamate, CRF and Substance P (increasing the likelihood of locus coeruleus firing) Inhibitory neurotransmitters: adrenergic, GABA, opiate and serotonin (decreasing the locus coeruleus firing) These neurotransmitters bind to locus coeruleus receptors
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Medication to reduce anxiety
* Two types of medication are most commonly used: * Benzodiazepines (e.g., Valium, Xanax) and anti-depressants * generally, antidepressants are preferred over benzodiazepines, because they tend to have less side effects (withdrawal symptoms, significant cognitive and motor side effects; increased risks of car accidents) * most people relapse when stop taking medications * Combining medication with psychological treatments: * in most anxiety disorders adding anxiolytics (benzodiazepines) to cognitivebehavioural treatment is not beneficial: people do not get the same chance to face their fears → exposure therapy may fail * Psychological treatments as the preferred treatment of most anxiety disorders (with possible exception of GAD)
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Exposure
Exposure: a person must face up to the source of their fear with the aim of extinction, which involves learning new associations with regard to the feared object → behaviourist view, but also used in CBT * Systematic desensitization in CBT: the client is first taught relaxation skills and is then confronted with a list of gradually more frightening stimuli (Wolpe, 1985) * CBT works well for 70-90% of clients * Effects of CBT endure at 6-month follow-up (Hollon et al., 2006), but long-term, many people experience some return of anxiety symptoms →Exposure should include as many features of the feared stimulus as possible →Exposure should be conducted in as many different contexts as possible * Flooding * New developments: virtual reality , internet-based programs * Mindfulness meditation skills: Taking a more reflective stance towards anxiety and emotions in general; relaxation
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Self-compassion linked to wellbeing
* Self-compassion linked to wellbeing * Reductions in anxiety, depression, stress, perfectionism, shame, body dissatisfaction, eating disorders * Improvements in happiness, life satisfaction, work satisfaction, optimism, social relationships * Self-esteem: linked to social comparison / own worth / success increases * Self-compassion not linked to being better than others. Not linked to success, stable sense of worth. * Linked to motivation: * Less fear of failure, more likely to try again and persist in efforts after failure * More personal responsibility and motivation to repair past mistakes * Linked to healthier behaviours: * More likely to eat well, more exercise. * Linked to improved relationships: * Those with high self-compassion are rated more positively by their partners * Not selfish! More giving, more caring, more loving, more compassionate, more supportive of autonomy, less angry.
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Compassion Focused Therapy
* CFT seeks to be a science based, integrative (consilient), evolution informed, biopsychosocial approach to the human mind. * CFT addresses the harmful-suffering causing aspects of our evolved minds via promoting caring relationships to self and others.
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Disgust - Insular Cortex
Thus, in other animals, the insula is about sensory disgust * In humans it’s also about moral disgust, which is intensely contextdependent * The insula is central to human tendency to consider what is merely different to be disgustingly wrong and to tell the amygdala about it
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Evolution of Minds
Charles Darwin The process of change via natural selection from the challenges of survival and reproduction. The three challenges (protection, resource acquisition, rest and digest) of life and four functions (motives, emotions, reasoning, behaviours) of the mind
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What is compassion?
A sensitivity to the suffering/distress of self and others with a commitment to try to alleviate and prevent it
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Three systems (Gilbert, 2009)
Many of us spend the majority of our time in threat and drive, which can lead to imbalanced emotions and distress. Soothing system - affiliating and reassuring its function: slow down, soothe, rest and digest, safeness, kindness, care etc Drive system - Motivation and resource seeking function: achieve goals, consume, accomplish tasks Threat system - Threat detection and protection function: manage threats, protection, survive and seek safety
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Shame
Attention is on damage to self and reputation (inward) Feelings are of anxiety paralysis confusion emptiness – self -directed anger Thoughts focused on negative judgements of the ‘whole self’ Behaviours focused on submissive appeasement, escape, denial, avoidant displacement, self -harm
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Guilt
Attention is on hurt caused to the other (outward) Feelings are ones of sorrow, sadness and remorse Thoughts focused on the other, sympathy and empathy. Focus on behaviour – what one did Behaviours focused on genuine apologies, reparation, making amends
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Cognition-Emotion Mismatch
It is the emotion of the criticism that does the damage, not the criticism itself
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What are personality traits?
A largely innate predisposition towards similar behaviours across situations and time
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The five factor model of personality
* “The Big Five” * Neuroticism * Extraversion * Openness to Experience * Agreeableness * Conscientiousness
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Personality traits and mental health
A meta-analysis of 175 studies (1980-2007) on the relationship between the Big Five personality traits and specific depressive, anxiety, and substance use disorders: * Neuroticism – high scores across all mental health problems * Extraversion – low score for depression and social anxiety * Openness to experience – no relationship * Agreeableness – low score for substance misuse * Conscientiousness – low scores across all mental health problems
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Neuroticism
* The general tendency to experience negative affects such as fear, sadness, embarrassment, anger, guilt, and disgust (Costa & McCrae, 1992) * Neuroticism predicts onset of Common Mental Disorders controlling for most (but not all) psychiatric confounders * Items used to assess neuroticism partially overlap with CMD symptoms, especially for internalising disorders * Neuroticism and CMDs share substantial but not all genetic and environmental determinants * Neuroticism has higher temporal stability than CMD symptoms, although the difference is smaller than commonly thought * Neuroticism probably moderates the impact of life stress on CMD; and * Reductions in neuroticism may partially mediate the effect of treatment on CMDs
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What are personality disorders?
Only when personality traits are inflexible and maladaptive and cause significant functional impairment or subjective distress do they constitute personality disorders * “A personality disorder is an enduring pattern of inner experience and behaviour * That deviates markedly from the expectations of the individual’s culture * Is pervasive and inflexible * Has an onset in adolescence or early adulthood * Is stable over time, and * Leads to distress or impairment”
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Personality Disorder Clusters - Odd/Eccentric
* Paranoid * Schizoid * Schizotype
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Personality Disorder Clusters - Dramatic/Erratic
* Antisocial * Borderline * Histrionic * Narcissistic
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Personality Disorder Clusters - Anxious/Fearful
* Avoidant * Dependent * Obsessive-compulsive
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Gender ratio in diagnosis
Obsessive compulsive (higher in females) Narcissistic (higher in males) Schizotypal (higher in males) Avoidant (higher in females) Antisocial (higher in males) Borderline (higher in females)
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Alternative DSM-5 model for PDs
* Criteria: * Significant impairments in self and interpersonal functioning * At least one pathological personality trait domain or facet * Personality impairments are persistent and pervasive * Personality impairments are not explained by developmental stage, sociocultural environment, substance abuse, another psychological or a medical condition
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Advantages of the Alternative DSM-5 model
* Clinicians can further specify which personality traits are of most concern for a given client * The dimensional scores provide a richer sense of detail than do the PD diagnoses * Personality trait ratings tend to be more stable over time than are PD diagnoses and are significantly related to many aspects of psychological adjustment, physical and mental health, and social outcomes!
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Antisocial Personality Disorder
People with ASPD display a long-term pattern of: * Disregarding the law * Violating the rights of others * Manipulating and exploiting others * Reckless acts for personal profit or pleasure and without remorse * They may do the following: * Justify or rationalise their behaviour * Blame the victim for being foolish or helpless * Be indifferent to the harmful effects of their actions on others
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Antisocial Personality Disorder - Diagnostic Criteria
* A pervasive pattern of disregard for and violation of the rights of others, since age 15 years, as indicated by three (or more) of the following: 1) Failure to conform to social norms concerning lawful behaviours, such as performing acts that are grounds for arrest. 2) Deceitfulness, repeated lying, use of aliases, or conning others for pleasure or personal profit. 3) Impulsivity or failure to plan. 4) Irritability and aggressiveness, often with physical fights or assaults. 5) Reckless disregard for the safety of self or others. 6) Consistent irresponsibility, failure to sustain consistent work behaviour, or honour monetary obligations. 7) Lack of remorse, being indifferent to or rationalising having hurt, mistreated, or stolen from another person. * The individual is at least age 18 years. * Evidence of conduct disorder typically with onset before age 15 years. * The occurrence of antisocial behaviour is not exclusively during schizophrenia or bipolar disorder.
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Borderline Personality Disorder (BPD)
* Instability of interpersonal relationships, self-image, affect, as well as marked impulsivity * The term “borderline” was first introduced in the US in 1938 to describe patients who were on the “border” between diagnoses DSM-5 Criteria: Presence of five or more of the following signs of instability in relationships, self-image, and impulsivity from early adulthood across many contexts: * Frantic efforts to avoid abandonment * Unstable interpersonal relationships in which others are either idealized or devalued * Unstable sense of self * Self-damaging, impulsive behaviors in at least two areas, such as spending, sex, substance abuse, reckless driving, and binge eating * Recurrent suicidal behavior or gestures or self-injurious behavior (e.g., cutting self) * Marked mood reactivity * Chronic feelings of emptiness * Recurrent bouts of intense or poorly controlled anger * During stress, a tendency to experience transient paranoid thoughts and dissociative symptoms
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Narcissistic Personality Disorder
DSM-5 Criteria Presence of five or more of the following signs of grandiosity, need for admiration, and lack of empathy from early adulthood across many contexts: * Grandiose view of one’s importance * Preoccupation with one’s success, brilliance, beauty * Belief that one is special and can be understood only by other high-status people * Extreme need for admiration * Strong sense of entitlement * Tendency to exploit others * Lack of empathy * Envy of others * Arrogant behaviour or attitudes
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Antisocial Personality Disorder - Neuroscience
Top down regulation/inhibition Reduction in prefrontal cortex activity (inability to plan, control and take responsibility) Hormones and Behaviour High levels of testosterone associated with many behaviours in this group (e.g high aggression, low empathy) Men commit more crimes than females Is testosterone a major cause of ASPD? - It is complicated Testosterone increases previously learnt aggression
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Psychopathy: Clinical Description
The concept long predates the DSM diagnosis of ASPD: Key characteristic is “poverty of emotions, both negative and positive” No sense of shame, lack of remorse and anxiety; do not learn from their mistakes, behave irresponsibly and often cruelly towards others Superficially charming - use that charm to manipulate others Antisocial behaviour is performed impulsively, as much for thrills as for financial or material gain
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Hare’s Psychopathy Checklist Revised (HPCR)
Self-report obviously people who are psychopaths have a tendency to lie 20 traits
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Decency et al. (2013)
fMRI study with psychopaths Imagine-self versus imagine-others conditions A normal response pattern was found for the imagine-self condition Significant reductions in activation in the areas associated with empathy for the imagine-others condition Significant increases in activation in the areas associated with pleasure and reward Skin conductance: Less reactive when confronted with an intense or aversive stimulus
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Psychopathy: Development of traits
Early behavioural warning signs of children at risk of psychopathy: Lack of remorse and guilt Lack of empathy Shallow affect Manipulation of others for own gain Sense of being more important than others These traits in combination are commonly known in the literature as “Callous-Unemotional” traits (CU traits) CU traits predict persistent, violent, and severe antisocial behaviour/psychopathy in adolescence and adulthood Somewhere between 25-50% children diagnosed with conduct problems show high callous-unemotional traits.
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What sets children apart with different levels of CU traits?
High CU traits: Engage in proactive aggression Lack guilt Do not worry about hurting others Often have low levels of anxiety Low CU traits: Often aggress when feel under threat Feel bad about hurting others Can have high levels of anxiety Children with high CU traits and conduct problems Lack of recognition and reactions to other people’s emotions Report feeling less fear themselves Less responsive to punishment Children with low CU traits and conduct problems: Emotionally overactive Hostile attribution bias - see threat in stimuli that typical children would not
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Biological differences in children
fMRI studies on the amygdala: Children with High CU traits and conduct problems: Low amygdala activity Typical children somewhere in the middle Children with Low CU and conduct problems: Higher amygdala activity
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Specific genes for emotional dysregulation
MAOA gene Has been linked to increased aggression and impulsivity (this gene affects serotonin and dopamine metabolism, influencing emotional regulation) Serotonin Transporter Gene (5-HTTLPR) “Short” allele is associated with increased aggression and emotional dysregulation, especially when paired with childhood adversity (influences serotonin uptake, affecting mood and impulse control) DRD2 & DRD4 (dopamine receptor genes) Influence dopamine signalling, which is crucial in reward processing and behavioural reinforcement Linked to impulsivity, risk taking and sensation-seeking behaviours COMT Gene Affects dopamine breakdown in the PFC. Variants on this gene associated with higher impulsivity and risk-taking
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Treatment of Antisocial Personality Disorder
There is a widely held belief that ASPD is untreatable The evidence base for psychological treatments for ASPD is as limited as that for pharmacological treatments A key issue in the treatment of ASPD is the test of the therapeutic outcome: how will the practitioner know if the treatment has been successful?
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Aetiology of Borderline Personality Disorder
Highly heritable (behavioural genetics: 60-70% Decreased functioning of serotonin system Increased activation of amygdala
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Social Environmental Factors - BPD
Parental separation, verbal and emotional abuse during childhood Linehan (1987): Biological vulnerability and being raised in a family environment that is invalidating
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Marsha Linehan - Dialectical Behaviour Therapy (DBT)
Problem solving and validation are the key approaches Some arguments that the name borderline creates stigma and should be changed to emotional dysregulation
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BPD treatment
Difficult to treat Interpersonal problems play out in therapy Attempts to manipulate the therapist Medications - these are symptom driven specific to each patient Antidepressants Mood stabilisers Dialectical Behavioural Therapy (Linehan, 1987) Acceptance and empathy plus CBT Emotion-regulation techniques Social skills training Mentalisation-based therapy Fail to think about their own and other’s feelings Schema-focused cognitive therapy Identify maladaptive assumptions that underlie cognitions
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Aetiology of NPD (Narcissistic Personality Disorder)
Milon (1996) hypothesised that parents who are overly indulgent promote children’s beliefs that they are special (even more special than other children) Parental tendencies to see their children as highly superior to others predicted an increase in their children’s narcissistic traits Child abuse or neglect Moderate genetic component (40-50% heritability), similar to other personality disorders Studies suggest a genetic link to temperament traits, such as high extraversion, low agreeableness, and high impulsivity Dopamine dysregulation - increased reward sensitivity, reinforcing grandiose behaviour and attention-seeking Lower oxytocin levels - may contribute to reduced emotional bonding and empathy Evolutionary perspective: Traits associated with NPD (dominance, status seeking, low empathy) may have evolved to enhance social competition and leadership ability
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Psychological factors for NPD
Fragile self-esteem: individuals with NPD often swing between grandiosity and feelings of worthlessness Defensive grandiosity: Grandiosity may be a defence mechanism against shame or rejection Cognitive distortions: Black and white thinking, externalising blame and exaggerated self-importance
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What is backdraft?
Backdraft - you make a big breakthrough in therapy and a realisation of change
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What are social factors that contribute to NPD?
Parenting styles and family dynamics Excessive praise without accountability - reinforces grandiosity and entitlement Harsh criticism or emotional neglect - leads to overcompensation with narcissistic defences
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What are cultural factors that contribute to NPD?
Western individualistic societies - prioritise success, status, and self promotion Social media and celebrity culture - rewards self-admiration, attention seeking, superficial validation
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What are peer influences and early socialisation that contribute to NPD?
Bullying or social rejection - may reinforce a compensatory need for superiority Highly competitive environments - narcissistic traits as a means of success and survival
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Social exclusion and NPD
Social exclusion Narcissistic traits leads to more activation of those pain-relevant neural regions That is, those with narcissistic tendencies were particularly sensitive to negative social interactions and may experience more intense social pain Could be linked to self-esteem and how much their self-esteem depends on external feedback
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Treatment of NPD
Challenging to treat because individuals lack insight into their behaviour and may be resistant to change May idealise or devalue the therapist, leading to treatment resistance Emotional vulnerability: confronting shame, inadequacy and rejection sensitivity can be deeply uncomfortable CBT - can help challenge entitlement/rigid beliefs DBT - less common but can help with aggression and emotion regulation CFT - trauma focused, shame focused, but also development of self-compassion and compassion for others, and can address self-worth and rejection sensitivity Many people enter treatment for other reasons (substance abuse, depression) Clinicians are encouraged to consider whether personality disorders are present because their presence predicts slower improvement in psychotherapy Psychotherapy is often the treatment of choice for personality disorders Tends to take more time - be more intense therapy Cognitive therapy - challenge maladaptive cognitions CFT - still requires more research
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Medication for Personality Disorders
Symptom driven approach - Anti-depressants (e.g SSRI's) for mood dysregulation, anxiety, and impulses Mood stabilisers (e.g Lithium) for impulsivity, aggression and mood swings Anti-anxiety medications (e.g benzos) for social anxiety, hyperarousal and panic symptoms Antipsychotics for emotional dysregulation, paranoia, and impulsivity
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Personality Disorders - Clinical challenges
No pure case - may emphasise the need to move away from standard classification system (alternative model)? High dropout rates in therapy Difficulties in establishing a therapeutic relationship Deeply ingrained patterns of thinking, feeling and behaving in these groups